Alzate et al.

Int J Clin Cardiol 2015, 2:9

ISSN: 2378-2951

International Journal of
Clinical Cardiology
Case Report: Open Access

Electrocardiographic Changes in Primary Hyperparathyroidism

Alexander Alzate1, Marcela Muñoz Urbano2* and Kenny Buitrago-Toro2
Faculty of Health Sciences, Internal Medicine department, Universidad Tecnológica de Pereira, Pereira, Risaralda,
1

Colombia
2
Faculty of Health Sciences, Medicine program, Universidad Tecnológica de Pereira, Pereira, Risaralda, Colombia

*Corresponding author: Marcela Muñoz Urbano, Faculty of Health Sciences, Medicine program, Universidad
Tecnológica de Pereira, 660003 27th avenue #10-02 Alamos neighborhood, Pereira, Risaralda, Colombia, E-mail:
marcemu_02@hotmail.com

hormone (PTH) in 1900 pg/mL (reference value: 10-60 pg/ml) and

Abstract
Electrolytic variability modifies normal structures of segments
and intervals on the electrocardiogram (ECG). We present a
case that was referred to the Internal Medicine department by
the Neurosurgery division for several pathological fractures.The
electrocardiogram led us to a diagnostic approach and finally we
show how electrocardiographic tracing changed after a treatment
implementation. Finally, in this study we highlight the importance of
an electrocardiogram on a patient´s approach.
Keywords
Hypercalcemia, Electrocardiogram, Hyperparathyroidism
A 43-year old African-Colombian man with personal clinical
history of arterial hypertension and urolithiasis was referred by the
Neuro surgery and Spine Surgery service to the Internal Medicine
and Hematology Department with a 6-year medical history of joint
pain in knees, elbows, hips, cervical and thoracolumbar spine. There
was no history of synovitis. The patient showed weakness at the
lower limbs with evidence of chest, thoracolumbar spine and leg
deformities that caused gait limitations and made a wheelchair for
mobilization necessary. Three years ago, he had a right femoral neck
fracture due to a fall from his own height which required surgical
fixation. He has been treated by Neuro-surgery and Spine Surgery
because of multiple vertebral fractures and a diffuse alteration in the
intensity of bone marrow. The patient was never subjected to studies
of his symptomatology, partly because he lived far from any major
city where he could undertake related treatment. In figure 1, an
admission ECG is shown.
It shows sinus rhythm at 110 beats per minute, normal axis, left
ventricular hypertrophy, normal PR and QRS length, QT 230 ms,
Short QTc 320 ms, Q-waves in V3 and an ST elevation in V2-V4.
phosphorus levels 2,7 mg/dL (reference value: 3-4.5 mg/dl). The
patient underwent thyroid ultrasound that showed a hypoechoic
heterogeneous lesion and well demarcated measuring 25 × 23 × 18
mm. Later, parathyroid scintigraphy was performed, which revealed
an abnormal accumulation of radiotracer in the left thyroid lobe. The
patient received a clinical diagnosis of primary hyperparathyroidism
(PHPT) secondary to hyperfunctioning parathyroid adenoma.
Therapy with zoledronic acid was started and he was referred to the
Head and Neck Surgery and Oncology department, just for surgical
removal of a solitary parathyroid tumor or subtotal resection of all
pathologic parathyroid tissue. The report of pathology in which the
diagnosis would be confirmed has not yet been provided. The last
ionized calcium measurement was 1.8 mmol/L. Control ECG is
shown in figure 2.
This control ECG shows sinus rhythm at 80 beats per minute,
normal axis, left ventricular hypertrophy, normal PR and QRS length,
QT 320 measured at DII, QTc 350 ms, and an ST elevation in V2-V5.
Discussion
Primary hyperparathyroidism is the most common etiology for
the hypercalcemia diagnosis that was made in this case. To determine
the presence of primary hyperparathyroidism the clinician must
prove an elevated or inappropriately normal serum level of intact
PTH associated hypercalcemia [1]. Many patients with primary
hyperparathyroidism are asymptomatic. Our patient presented with
a variety of chronic symptoms and signs, including renal, bone,
neurological and cardiovascular manifestations [1-4]. The disease is
commonly manifested with hypertension, low bone mineral density
and consequently an increased rate of fractures; all of which were
shown in this patient [2].

Numerous studies were performed. A bone scintigraphy revealed
multiple abnormal accumulations of radiotracer affecting the
thoracic and lumbar vertebral bodies and diffuse widespread uptake.
Initial ionized calcium level was 2.02 mmol/L (reference value: 1.1-
1.4 mmol/liter), serum calcium in 13.2 mg/dL (reference value: 9.0-
10.5 mg/dl), serum creatinine1.1 mg/dL (reference value: <1.5 mg/
dl), urea nitrogen 17 mg/dl (reference value:10-20 mg/dl), parathyroid
It is well known that potential action in cardiac cells is generated
by the movement of electrolytes across the cardiac cell membrane
and abnormal ion’s levels may lead to altered electrical activity.
Hypercalcemia may induce electrocardiogram abnormalities such
as QT interval shortening, sometimes associated with prolongation
of PR segment and QRS interval, increased duration of the T-wave,
decreased T-wave amplitude and prominent U-waves [3,5].

Citation: Alzate A, Urbano MM, Buitrago-Toro K (2015) Electrocardiographic Changes in

Primary Hyperparathyroidism. Int J Clin Cardiol 2:068
ClinMed Received: October 14, 2015: Accepted: December 12, 2015: Published: December 15, 2015
Copyright: © 2015 Alzate A, et al. This is an open-access article distributed under the terms
International Library of the Creative Commons Attribution License, which permits unrestricted use, distribution,
and reproduction in any medium, provided the original author and source are credited.
 Figure 1: Admission ECG. Which electrolyte abnormality is shown in this tracing?

In our case, the PR segment was normal as well as QRS complex.
However, it has been described that the amplitude of the QRS
decreased as the ionized calcium level decreased, and the presence of
short QTc has also reverted once the hypercalcemia has been corrected.
The abnormal short QTc that was evidenced in the first ECG was not
shown in the second tracing, with a QTc of 355 ms as is shown in
figure 2 [4,6]. It has been reported in previous cases that patients who
underwent a surgical remove of adenoma as the cause of primary
hyperparathyroidism, recover normal ionized calcium levels as well
of ECG regular features. Our patient’s parathyroid adenoma has not
been resected but his calcium ionized levels decreased considerably
and this was reflected on the control ECG tracing [7]. On the ECG,
the lower limit for the duration of QTc is not well established but it
is reasonable to consider a normal QTc interval between 360 ms and
450 ms in males and 370 ms to 470 ms in females [4,8].
The patient never reported thoracic pain and cardiac enzymes
taken initially were negative. It is important to mention this since
the ECG showed ST elevation in V2-V4 which could correspond to
myocardial ischemia, a finding that has been reported in some similar
cases with hypercalcemia [4].
In this case, the presence of J waves which occur in certain
conditions like hypothermia, early repolarization and, the Brugada
syndrome could be observed. These findings are most prominent
in precordial leads V2 to V5. In the patient, they are clearer in the
second tracing when the calcium level was lower but still high, so
it is difficult to distinguish between early repolarization and real
Osborn waves since those waves are commonly correlated with severe
hypercalcemia [6].
On the other hand, the ECG evidenced signs of left ventricular
hypertrophy (according to Sokolow criteria). The patient did not
have an echocardiogram for demonstrating any left ventricular

Alzate et al. Int J Clin Cardiol 2015, 2:9 ISSN: 2378-2951 • Page 2 of 3 •
 Figure 2: Control ECG.
hypertrophy but this could be related to the presence of chronic
hypertension which is one of many cardiovascular manifestations of
hyperparathyroidism [1,8].
As we mentioned before, the patient was referred to the Head and
Neck Surgery and Oncology department for operative management
which is currently the only curative therapy and is clearly indicated
for all patients with classic symptoms or complications of PHPT, as
in this case. The patient met criteria for surgical management such as
< 50 years of age, inability to participate in an appropriate follow up,
and complications of PHPT that unfortunately were associated to a
chronic unattended illness [9].
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